Snyder-Theilen feline sarcoma virus (ST-FeSV)- or Abelson murine leukemia virus (A-MuLV)-transformed mink cells exhibit a relatively high reversion rate compared to the nontransformed phenotype. The phenotypically normal cells have not rearranged the integrated retrovirus. However, it could be demonstrated that the retroviral sequences, in comparison with those in transformed cells, are highly methylated. These findings demonstrate that viral oncogene-mediated transformation can be regulated by methylation. Acute promyelocytic leukemia is frequently associated with a reciprocal 15-17 chromosomal translocation. The c-fes oncogene, which has been mapped to chromosome 15, was shown to be translocated to chromosome 17 in this disease. Using a probe specific for v-fms, a human cosmid library was screened for v-fms homologous sequences. A contiguous region of cellular DNA of approximately 64 kilobases (kb) in length was isolated. Within this region of the DNA, v-fms homologous sequences are dispersed over a total region of around 32 kb and represent the entire human cellular homolog of v-fms. By analysis of human-mouse somatic cell hybrids, human c-fms could be localized to chromosome 5 band q34. This chromosomal localization is of interest in view of reports of a specific deletion involving approximately two thirds of the q arm of chromosome 5 in acute myelogenous leukemia.